Antiphospholipid antibodies are strongly associated with arterial and
venous thrombosis and with fetal loss. Recently an experimental model for
antiphospholipid syndrome (APLS) was established in our laboratory. In this model, mice are immunized passively or actively with
anticardiolipin antibodies and acquire the syndrome, which is characterized by prolonged activated partial thromboplastin time (APTT),
thrombocytopenia, low fecundity rate, and fetal loss. In a normal process of pregnancy,
lymphokines affect fetal implantation and development.
Cytokines from the
colony stimulating factor family, like
GM-CSF and
IL-3, were shown to be positive signals for implantation and to promote placental development and fetal growth. Given our preliminary findings of low
IL-3 in mice with APLS and the efficacy of
IL-3 in preventing fetal loss in a strain of mice prone to
fetal resorption, our aim in the present study was to examine the effect of murine recombinant
IL-3 (mrIL-3) on pregnant mice induced with experimental APLS. Mice were passively transfused to the tail vein, 24 h following mating, with
anticardiolipin antibodies. The mice were divided into two groups: one group was injected intraperitoneally with mrIL-3 on days 6.5, 8.5, and 10.5 after mating, while the control group was injected with PBS. When the mice were killed on day 15 of pregnancy a 32% +/- 4.2 resorption rate was observed in the anti-
cardiolipin-immunized group, which was reduced to 4% +/- 0.3 following treatment with mrIL-3. The
thrombocytopenia associated with the experimental APLS was also corrected following lymphokine administration.
IL-3 may be effective in prevention of recurrent fetal loss in APLS.